2023-09-05 00:04:25
University of Bern Researchers Discover Mechanism That Promotes Spread of Yeast Fungal Infections
Blood poisoning caused by fungal infections is a life-threatening danger, and researchers at the University of Bern have made a significant breakthrough in understanding how a yeast fungus spreads within the body. This discovery could pave the way for new therapeutic options in the treatment of blood poisoning caused by yeast fungi, as well as other internal fungal infections.
The yeast fungus Candida albicans is typically harmless and resides on our mucous membranes without causing any issues. However, when the immune system is compromised, such as in individuals with diseases like AIDS or those taking medication that suppresses the immune system, the fungus can become dangerous. Surgical interventions that damage the mucosal barrier in individuals with a healthy immune system can also promote the spread of Candida albicans, leading to blood poisoning and potential organ damage.
The immune system plays a crucial role in the body’s response to invading pathogens and involves an inflammatory response. A specific protein called interleukin 1 receptor antagonist acts as a natural antagonist to the pro-inflammatory signaling substance interleukin 1, preventing uncontrolled inflammatory reactions.
However, a recent study led by PD Dr. Stefan Freigang from the Institute of Tissue Medicine and Pathology at the University of Bern suggests that this anti-inflammatory protein actually promotes the spread of Candida albicans. The study found that the protein, produced by scavenger cells known as macrophages, inhibits the production and swarming of neutrophils, a subset of white blood cells that play a crucial role in the early defense against infection.
In mice, the researchers observed that genetically bred mice that did not produce the anti-inflammatory proteins had an intact arsenal of neutrophils and were able to combat Candida albicans infections successfully. In contrast, normal mice that produced the anti-inflammatory proteins had inhibited neutrophils, allowing the fungi to spread. Surprisingly, the loss of the anti-inflammatory proteins did not lead to an overshoot of the inflammatory response but rather a reduction.
The implications of this research could lead to new therapeutic approaches to treat fungal sepsis, which currently has a high mortality rate. By targeting the specific protein that promotes the spread of yeast infections, scientists hope to develop more effective treatment strategies. The researchers plan to use patient samples to confirm their observations from the mouse model and investigate whether the protein also promotes Candida albicans infections in humans.
The study’s findings were published in the journal Immunity, offering hope for improved treatments for blood poisoning caused by yeast fungi and other internal fungal infections.
Source: University of Bern]
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